Veel T, Buanes T, Engeland E, Raeder M G
University of Oslo, Institute for Experimental Medical Research, Norway.
Acta Physiol Scand. 1990 Apr;138(4):487-95. doi: 10.1111/j.1748-1716.1990.tb08876.x.
Secretin stimulation clears the cytoplasm of intralobular pancreatic duct cells in pigs of tubulovesicles and causes these cells to secrete HCO3- into the pancreatic juice. To determine whether the clearance of cytoplasmic tubulovesicles involves the microtubule system and is important for initiation of HCO3- secretion, the effect of the microtubule poison colchicine on duct cell morphology and pancreatic HCO3- secretion was measured in anaesthetized pigs. Before colchicine, secretin reduced the density of tubulovesicles in the cytoplasm of pancreatic duct cells from 92 +/- 8 U to 8 +/- 2 U and initiated pancreatic secretion of 176 +/- 21 mumols min-1 HCO3-. After colchicine, secretin failed to lower duct cell tubulovesicle density and caused the secretion of only 77 +/- 14 mumols min-1 HCO3-. By contrast, lumicolchicine, an isomer of colchicine that does not affect microtubules, did not inhibit pancreatic HCO3- secretion. Colchicine did not reduce carbonic anhydrase or Na,K-ATPase activities in in-vitro assays. The clearance of tubulovesicles from the cytoplasm of pancreatic duct cells therefore seems to be microtubule-dependent and important for the pancreatic HCO3- secretion.
促胰液素刺激可使猪的小叶内胰管细胞胞质中的微管泡清除，并使这些细胞向胰液中分泌HCO₃⁻。为了确定胞质微管泡的清除是否涉及微管系统以及对HCO₃⁻分泌的起始是否重要，在麻醉的猪中测量了微管毒物秋水仙碱对导管细胞形态和胰腺HCO₃⁻分泌的影响。在使用秋水仙碱之前，促胰液素使胰管细胞胞质中微管泡的密度从92±8 U降至8±2 U，并引发胰腺以176±21 μmol·min⁻¹的速率分泌HCO₃⁻。使用秋水仙碱后，促胰液素未能降低导管细胞微管泡密度，仅导致以77±14 μmol·min⁻¹的速率分泌HCO₃⁻。相比之下，秋水仙碱的异构体光秋水仙碱不影响微管，也不抑制胰腺HCO₃⁻分泌。在体外试验中，秋水仙碱并未降低碳酸酐酶或钠钾ATP酶的活性。因此，胰管细胞胞质中微管泡的清除似乎依赖于微管，并且对胰腺HCO₃⁻分泌很重要。
